PMID- 37454529
OWN - NLM
STAT- MEDLINE
DCOM- 20230821
LR  - 20230821
IS  - 2213-2317 (Electronic)
IS  - 2213-2317 (Linking)
VI  - 65
DP  - 2023 Sep
TI  - Antioxidant mitoquinone suppresses benign prostatic hyperplasia by regulating the 
      AR-NLRP3 pathway.
PG  - 102816
LID - S2213-2317(23)00217-3 [pii]
LID - 10.1016/j.redox.2023.102816 [doi]
LID - 102816
AB  - Mitoquinone (MitoQ), a mitochondria-targeted antioxidant, has been used to treat 
      several diseases. The present study aimed to investigate the therapeutic effects 
      of MitoQ in benign prostatic hyperplasia (BPH) models and their underlying 
      molecular mechanisms. In this study, we determined that MitoQ inhibited 
      dihydrotestosterone (DHT)-induced cell proliferation and mitochondrial ROS by 
      inhibiting androgen receptor (AR) and NOD-like receptor family pyrin 
      domain-containing 3 (NLRP3) signaling in prostate epithelial cells. Molecular 
      modeling revealed that DHT may combine with AR and NLRP3, and that MitoQ inhibits 
      both AR and NLRP3. AR and NLRP3 downregulation using siRNA showed the linkage 
      among AR, NLRP3, and MitoQ. MitoQ administration alleviated pathological prostate 
      enlargement and exerted anti-proliferative and antioxidant effects by suppressing 
      the AR and NLRP3 signaling pathways in rats with BPH. Hence, our findings 
      demonstrated that MitoQ is an inhibitor of NLPR3 and AR and a therapeutic agent 
      for BPH treatment.
CI  - Copyright (c) 2023. Published by Elsevier B.V.
FAU - Jin, Bo-Ram
AU  - Jin BR
AD  - Department of Oriental Pharmaceutical Science, College of Pharmacy, Kyung Hee 
      University, Seoul, 02447, Republic of Korea.
FAU - Lim, Chae-Young
AU  - Lim CY
AD  - Department of Life Science, Dongguk University-Seoul, 32 Dongguk-ro, 
      Ilsandong-gu, Goyang-si, Gyeonggi-do, 10326, Republic of Korea.
FAU - Kim, Hyo-Jung
AU  - Kim HJ
AD  - Department of Oriental Pharmaceutical Science, College of Pharmacy, Kyung Hee 
      University, Seoul, 02447, Republic of Korea.
FAU - Lee, Minho
AU  - Lee M
AD  - Department of Life Science, Dongguk University-Seoul, 32 Dongguk-ro, 
      Ilsandong-gu, Goyang-si, Gyeonggi-do, 10326, Republic of Korea. Electronic 
      address: MinhoLee@dgu.edu.
FAU - An, Hyo-Jin
AU  - An HJ
AD  - Department of Oriental Pharmaceutical Science, College of Pharmacy, Kyung Hee 
      University, Seoul, 02447, Republic of Korea; Department of Integrated Drug 
      Development and Natural Products, Graduate School, Kyung Hee University, Seoul, 
      02447, Republic of Korea. Electronic address: hjan@khu.ac.kr.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20230711
PL  - Netherlands
TA  - Redox Biol
JT  - Redox biology
JID - 101605639
RN  - 0 (Antioxidants)
RN  - 47BYS17IY0 (mitoquinone)
RN  - 0 (Receptors, Androgen)
RN  - 0 (NLR Family, Pyrin Domain-Containing 3 Protein)
SB  - IM
MH  - Male
MH  - Humans
MH  - Rats
MH  - Animals
MH  - *Prostatic Hyperplasia/drug therapy/genetics/chemically induced
MH  - Antioxidants/pharmacology/therapeutic use
MH  - Receptors, Androgen/genetics/metabolism
MH  - NLR Family, Pyrin Domain-Containing 3 Protein/genetics
PMC - PMC10368918
OTO - NOTNLM
OT  - Androgen receptor
OT  - Benign prostatic hyperplasia
OT  - Dihydrotestosterone
OT  - Mitoquinone
OT  - NLRP3
COIS- Declaration of competing interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2023/07/17 00:42
MHDA- 2023/08/21 06:43
PMCR- 2023/07/11
CRDT- 2023/07/16 18:05
PHST- 2023/06/14 00:00 [received]
PHST- 2023/06/30 00:00 [revised]
PHST- 2023/07/10 00:00 [accepted]
PHST- 2023/08/21 06:43 [medline]
PHST- 2023/07/17 00:42 [pubmed]
PHST- 2023/07/16 18:05 [entrez]
PHST- 2023/07/11 00:00 [pmc-release]
AID - S2213-2317(23)00217-3 [pii]
AID - 102816 [pii]
AID - 10.1016/j.redox.2023.102816 [doi]
PST - ppublish
SO  - Redox Biol. 2023 Sep;65:102816. doi: 10.1016/j.redox.2023.102816. Epub 2023 Jul 
      11.